Founder is the common name for laminitis, a condition defined as inflammation of the laminae within the hoof. It can cause lameness in horses, ponies and donkeys and involves damage to the laminar connection between the hoof wall and the coffin bone.
This may lead to rotation and/or sinking of the coffin bone, which causes severe pain and can permanently damage the hoof structure. Horses with the condition may show various signs of distress and discomfort and typically cannot move about comfortably.
The term founder is often used in the context of a horse that has chronic (long-term) or repeated laminitis episodes, but horses can have a single episode of founder or laminitis.
There are multiple risk factors for the development of founder, but over 90% of cases are caused by high insulin (hyperinsulinemia), Equine Metabolic Syndrome (EMS) and Cushing’s disease (PPID). Many other risk factors are involved and will be discussed in further detail below.
Prevention and treatment of founder involve addressing the underlying causes of the condition and require a lot of dedication from the horse owner. Founder is not always treatable if the internal structures of the foot have sustained significant damage but the vast majority can be saved with elimination of the cause and correct hoof care.
Proper feeding, hoof care, and management are critical for supporting hoof health. If your horse is recovering from or at risk of founder, our nutritionists can help you develop a balanced feeding plan to address laminitis risk and optimize hoof health.
What is Founder?
A debilitating and painful condition, founder affects the laminae and the coffin (pedal) bone in the equine foot.
The laminae are the two layers of finger-like protrusions that interlock or interdigitate with each other like Velcro to form the structure that holds the hoof wall onto the internal structures. The laminae also help support the coffin bone.
The coffin (pedal or P3) bone is the bone that rests in the cradle of the hoof, and it plays a key role in hoof form and function. It is the first bone in the boney column of the leg to absorb the shock of the footfall, and its proper function is critical to limb circulation. 
To confirm a diagnosis of founder, your veterinarian will conduct clinical and radiographic examination of the hooves and the entire horse.  In the physical exam, your veterinarian will look for signs of current and chronic (ongoing) laminitis while also investigating hoof structure and causes for the episode.
Radiographs show the degree of coffin bone rotation, coffin bone sinking (also known as distal descent), sole and wall thickness, toe length and, sometimes, concurrent abscesses. This information can help your veterinarian, farrier and nutritionist work together to relieve your horse’s pain with corrective foot care, feed changes, housing changes and medications.
Laminitis vs. Founder
The terms “laminitis” and “founder” are often used interchangeably by horse owners. However, a distinction can be made between the acute phase of laminitis versus ongoing chronic issues.
Acute laminitis or a “bout of laminitis” typically refers to the sudden onset of pain related to weakening of the laminae.
The term founder is often used colloquially to refer to the ongoing condition when it involves rotation/sinking of the coffin bone. 
Not all horses with acute laminitis will experience coffin bone rotation. However, many horses with founder will have previously had one or more attacks of laminitis. Once a horse has had one episode, it is usually at risk of reoccurrence.
Each horse hoof contains approximately 600 laminae forming two interlocking layers that provide structural support to the hoof. The laminae connect the hoof wall to the coffin bone within the hoof.
When the laminae become weakened, the following can result:
- Separation of the sole from the hoof wall observed at the white line of the hoof; the area between the wall and sole of the hoof
- Flat hoof sole
- Divergent hoof rings
- Acute Laminitis
- Founder/Chronic Laminitis
During acute laminitis episodes of non-metabolic causes, several factors contribute to damage to the laminae. Toxins can activate matrix metalloproteinase enzymes. The tissues are invaded by white blood cells in an inflammatory response. Blood supply is compromised either as an initial event or later on secondary to tissue swelling and clot formation.
In metabolic / endocrinopathic laminitis, the inflammatory features of white cell infiltration and enzyme activation are not present but there are elevated levels of the potent vasoconstrictor endothelin-1 suggesting blood flow is compromised. 
A laminitis attack can lead to the death of cells in the laminae as well as cell proliferation. If there is enough damage, the laminae lose their strength, weakening this important structural component of the hoof.
In a hoof affected by founder, the laminae can become so damaged that they are unable to sufficiently anchor the coffin bone. The position of the coffin bone may drop (sink) under the weight of the horse and due to the upward pull of the flexor tendon attached to the base of the bone. 
This is known as coffin bone rotation. The degree of rotation is measured by taking radiographs of the hoof.
In advanced cases of founder, the coffin bone can protrude through the sole of the hoof.  At this stage, euthanasia is often considered because of the degree of nursing and prolonged period required for recovery but horses can recover from penetration.
Effects of Founder on the Foot
When rotation of the angle of the coffin bone occurs relative to the short pastern bone located above it, intense pressure is exerted on the sole of the foot potentially causing it to penetrate the sole.
A depression may be present at the front of the coronet where the joint space between the coffin and pastern bone becomes wider than normal. 
Prevalence and Prognosis
Half of all US horse operations surveyed in 1998 reported having at least one horse with lameness and 13% reported having a horse with laminitis.
The survey also found that 4.7% of horses with laminitis died or had to be euthanized due to the condition. 
In this owner-reported survey, over 50% of reported laminitis cases were thought to be due to grazing on lush pasture and grain overload.
Up to 74% of horses with laminitis recovered and were able to be used for their intended purposes.
A British study of equine veterinary clinics found that active laminitis cases represented one out of every 200 visits to veterinary practitioners. 
Common Causes of Founder
Founder is a complex condition that can be precipitated by both metabolic and environmental factors acting on their own or in combination with each other. 
Some of the most common causes of founder include the following.
The overconsumption of grain products as in the “horse broke into the feed room” scenario, and experimental overloads of chickory fructan can cause laminitis and founder.
Grains are high in hydrolyzable carbohydrates (HC), including sugar and starch. High intake of starch and sugar can overwhelm the small intestine and lead to excess carbohydrates reaching the hindgut, often called “starch overload”. A similar scenario can be created experimentally with unnaturally large doses of pure chicory root fructan given by stomach tube.
This leads to higher levels of lactic acid production in the cecum and colon. If the the pH drops below 6, a condition known as hindgut acidosis develops.
An excessive amount of lactic acid in the hindgut can disrupt the microbial population and cause the death of fibre-fermenting hindgut microbes. As acid accumulates in the intestine, it also causes damage to the gastrointestinal lining. 
However, this is an extreme scenario requiring large overloads and is accompanied by fever, colic and diarrhea. Much smaller amounts of hydrolyzable carbohydrates can cause laminitis by increasing insulin in horses with EMS or PPID.
Absorption of Dietary Toxins
Horses with a compromised gastrointestinal lining absorb toxins into their bloodstream. A common source of toxins is bacterial exotoxins. 
Upon entering the bloodstream, these toxins lead to activation of matrix metalloproteinases (MMPs) that damage the hoof laminae.
Research investigating metabolism-related causes of laminar damage suggests that a sugar metabolite called methylglyoxal (MG) may be responsible for damage in the feet of horses. However, a study comparing horses with hyperinsulinemia t